Establishment of Experimental Mastitis Model by Lipopolysaccharide via Teat Duct in Rabbit

[ Objective] This study was conducted to explore the method of establishing Lipopolysaccharide （LPS） -induced mastitis pathological models and reveal dynamic pathological changes of mammary tissue before and after LPS perfusion, finally providing convenient animal models for establishing LPS- induced acute clinical mastitis researches. [ Method] Twelve lactating rabbits （the 7th day after parturition） were perfused with LPS into the fourth mammary gland via the teat duct. Exactly at 2h before perfusion, 6 h, 12 h, 24 h, 48 h, 72 h, 5 d and 7 d after, the indexes such as rectal temperature, total white blood calls and neutrophils, C -response protein （CPR） content and lactate dehydrogenase （LDH） activity were determined, respectively. Then the rabbits were euthanatized and the mammary glands were removed and fixed for histopathologic evalua- tions. [Result] The results showed that inflammatory cells were observed in mammary tissue 6 h after LPS perfusion, structure of mammary tissue disorderly at 24 h, self - regeneration after 48 h and back to normal at 7 d. LDH activity was increasing significantly （ P 〈 0.05） at 12 h （ P 〈 0.05）, peaking at 24 h, decreasing at 5 d （ P 〈 0.05） and returning to health at 7 d. CRP content was increasing significantly （ P 〈 0.05） at 6 to 72 h, pea- king at 12 h, decreasing at 48 h, back to normal at 5 d. [ Conclusion] The results suggested that the rabbit experimental mastitis model was suc- cassfullv constructed bv LPS Derfusion via teat duct.

Influence of periodontitis and nonsurgical periodontal intervention on atherosclerosis diseases

Objective: Periodontitis and atherosclerosis diseases are chronic inflammatory disorders which are highly prevalent in populations. Nonsurgical periodontal intervention belongs to the initial therapy strategy to periodontal diseases. Periodontal pathogen can enter into blood stream through the ulceration epithelial resulting in bacteraemia when periodontitis is severe. The objective is to investigate the relationship between periodontitis and atherosclerosis diseases, and the influence of nonsurgical periodontal intervention on atheroma and atherosclerosis diseases. Methods: This study reviewed and analyzed the papers which published in the world associated with periodontitis or periodontal intervention on atherosclerosis diseases. Results: Periodontitis and periodontal infectious are important risk factors for atherosclerotic diseases. Much evidence has proved the durative severe periodontitis can result in bacteraemia and systemic inflammation, elevated C-response protein in serum, gingival microcirculation changed, periodontal microorganism reproduced, and endothelial dys-function and endocarditis. Nonsurgical periodontal intervention can remove the pathogenesis bacteria and calculus to recover periodontal health. Effective periodontal therapy can reduce bacteraemia and stop the hurt to vessels. Nonsurgical periodontal therapy may interfere periodontal bacteria, inhibit inflammation response and C-response protein, improving gingival microcirculation and vessel epithelial function to prevent atherosclerosis. Conclusion: Nonsurgical periodontal intervention can improve or decrease the rate of atherosclerotic disease by interfere the severe periodontitis. The detailed mechanism of periodontal intervention on atheroma and atherosclerotic disease is still need to be explored.